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The ECF sigma factor SigT regulates actinorhodin production in response to nitrogen stress in Streptomyces coelicolor
in
Analysis
/ Antibiotics
/ Bacteria
/ Cloning
/ E coli
/ Gene expression
/ Genes
/ Metabolism
/ Metabolites
/ Mutation
/ Nitrogen
/ Plasmids
/ RNA polymerase
/ Stress
/ Studies
/ Trace elements
2011
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The ECF sigma factor SigT regulates actinorhodin production in response to nitrogen stress in Streptomyces coelicolor
by
in
Analysis
/ Antibiotics
/ Bacteria
/ Cloning
/ E coli
/ Gene expression
/ Genes
/ Metabolism
/ Metabolites
/ Mutation
/ Nitrogen
/ Plasmids
/ RNA polymerase
/ Stress
/ Studies
/ Trace elements
2011
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The ECF sigma factor SigT regulates actinorhodin production in response to nitrogen stress in Streptomyces coelicolor
in
Analysis
/ Antibiotics
/ Bacteria
/ Cloning
/ E coli
/ Gene expression
/ Genes
/ Metabolism
/ Metabolites
/ Mutation
/ Nitrogen
/ Plasmids
/ RNA polymerase
/ Stress
/ Studies
/ Trace elements
2011
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The ECF sigma factor SigT regulates actinorhodin production in response to nitrogen stress in Streptomyces coelicolor
Journal Article
The ECF sigma factor SigT regulates actinorhodin production in response to nitrogen stress in Streptomyces coelicolor
2011
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Overview
Sigma factors of the extracytoplasmic function (ECF) subfamily are important regulators of stress responses in bacteria. This work described the characterization of ECF sigma factor SigT in Streptomyces coelicolor. We found the absence of sigT almost abolished the production of the antibiotics actinorhodin (Act) under nitrogen stress. Under nitrogen-limited conditions, significantly reduced Act production and linked actII-ORF4 transcription with respect to wild type were observed in the sigT-null mutant. Using reporter (xylE) fusion to sigT promoter, we demonstrated that sigT was induced by nitrogen limitation in a SigT-dependent manner. Transcriptional analyses showed that SigT controlled the expression of relA, the ppGpp synthetase gene, and consequently affected the Act production upon nitrogen starvation. Co-transcription analysis revealed that sigT was co-transcribed with rstB (gene upstream of sigT) but not with rstA (gene downstream of sigT). Phenotypic and transcriptional results suggested RstA may modulate the activity of SigT positively.[PUBLICATION ABSTRACT]
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